Abstract
The localization of lipoprotein lipase (LPL) in human atherosclerotic lesions was studied with immunocytochemical techniques. In the fibrous cap and surrounding intima of the plaque, where the smooth muscle cell is the dominating cell type, a high number of cells reacted with anti-LPL. A much lower number of stained cells was seen in the central lipid core region where the macrophages dominate. Further characterization of the LPL-containing cells in tissue sections showed that most of them were smooth muscle cells. Only a minor fraction of the macrophages in the plaque contained the enzyme. The results were confirmed on isolated cells from atherosclerotic tissue. Lipoprotein lipase was also detected in smooth muscle cells of non-atherosclerotic arteries. These findings suggest that the smooth muscle cells are the major source of LPL in the vascular wall. However, the enzyme was not present in some of the smooth muscle cells in the atherosclerotic lesion. This may imply that LPL synthesis is down-regulated in the atherosclerotic plaque.
Highlights
The localization of lipoprotein lipase (LPL) in human atherosclerotic lesions was studied with immunocytochemical techniques
This study was made in order to identify LPL-containing cells in nonatherosclerotic and atherosclerotic human arteries by immunocytochemical techniques
The cells in the intima, including the endothelium, and in the media of nonatherosclerotic arteries reacted with anti-LPL
Summary
The localization of lipoprotein lipase (LPL) in human atherosclerotic lesions was studied with immunocytochemical techniques. Lipoprotein lipase was detected in smooth muscle cells of non-atherosclerotic arteries. These findings suggest that the smooth muscle cells are the major source of LPL in the vascular wall. The enzyme was not present in some of the smooth muscle cells in the atheroscleroticlesion This may imply that LPL synthesis is down-regulated in the atherosclerotic plaque.-Jonasson, L., G. Available data indicate that both major cell types in the atherosclerotic lesion may synthesize LPL. These data are derived from cell culture studies and it is unclear whether they are related to the actual in vivo situation
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